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GI Boards November 20th 2024 > Hepatology > Flashcards

Hepatology Flashcards

1
Q

Can non-hepatitis viruses (EBV, CMV, HSV, Influenza, COVID) that cause viral hepatitis, cause CHRONICITY?

A

NO!

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2
Q

Which VIRUS is the most COMMON cause of non-hepatitis virus ACUTE HEPATITIS?

A

EBV

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3
Q

Who is most SUSCEPTIBLE to VIRAL HEPATITIS from the non-hepatitis viruses (EBV, COVID, etc.)?

A

Children and Immunocompromised (HIV, Transplant, Chemotherapy)

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4
Q

Which HEPATITIS VIRUS has shown the greatest INCREASE in INCIDENCE over the past 10 years?

A

HAV (narcotics, homelessness)

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5
Q

What can SIMULTANEOUS CO-INFECTION with HBV & HDV cause?

A

Fulminant Hepatic Failure

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6
Q

What causes a HIGH-RATE of hepatitis CHRONICITY in patients infected with HBV?

A

HDV Superinfection (found in 40% of patients infected with HBV - immigrants)

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7
Q

If a patient from OUTSIDE the USA presents with HEPATITIS symptoms but tests for HAV, HBV, HCV are negative, WHAT should you test for next?

A

HEV (very prevalent outside the US - food) and in OLDER 60-80 age groups - FECES of PIG, SHEEP, WILD BOAR, DEER, FISH - genotypes III & IV - hunters, eating the meat, handling feces**

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8
Q

What PHASE of hepatitis infection is ASYMPTOMATIC and how long is it for HAV, HBV and HCV?

A

INCUBATION phase:
HAV (4 WEEKS)
HBV (3 MONTHS)
HCV (6 WEEKS)

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9
Q

What PHASE of hepatitis infection presents with FLU-LIKE symptoms (3-5 days), RUQ tenderness, LFT elevations and POSITIVE serology?

A

PRODROME

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10
Q

An UNCOMMON (<20%) hepatitis PHASE which can last DAYS to WEEKS?

A

ICTERIC

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11
Q

In which hepatits PHASE do the LFTs normalize and ANTIBODIES are formed?

A

RESOLUTION

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12
Q

Which HBV patients develop CHRONIC infection at a rate of 90% vs 5-10%?

A

INFANTS (vertical transmission)

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13
Q

Which hepatitis VIRUSES have the HIGHEST potential for CHRONIC infection?

A

HBV (INFANTS ONLY - 90% vs 5-10% adults)
HCV - 85%
HDV - 90% (only with SUPERINFECTION i.e. on top of HBV)

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14
Q

Which VIRAL hepatitis NEVER causes Acute Liver Failure?

A

HCV

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15
Q

Age >40, HAV/HEV or HBV, ALT >10,000, Bilirubin >10, elevated INR, ENCEPHALOPATHY?

A

ALF (Acute Liver Failure) 80% mortality without TRANSPLANT

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16
Q

What 2 factors increase RISK of ALF in HAV?

A
  1. Age >40
  2. CHRONIC liver disease
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17
Q

What FACTOR increases the RISK of ALF in HEV?

A

PREGNANCY

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18
Q

What 3 factors increase the RISK of ALF in HBV?

A
  1. Age >40
  2. Seroconversion (from viral infection to antibody production HBeAb, HBsAb)
  3. Superinfection with HDV
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19
Q

What are the COMMON EXTRAHEPATIC (immune-complex deposition) manifestations of HBV and HCV?

A

Cryoglobulinemia
Glomerulonephritis
Lichen Planus
Guillian Barre (HBV)
Polyneuropathy (HCV)

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20
Q

What are the UNIQUE EXTRAHEPATIC manifestations of HBV?

A

Polyarteritis Nodosa (PAN)
Bullous Pepnhigoid

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21
Q

What are the UNIQUE EXTRAHEPATIC manifestations of HCV?

A

Porphyria Cutanea Tarda (PCT)
DM-II
B-Cell Lymphoma

Porphyria Cutanea Tarda
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22
Q

Arthritis, Adult Still Disease and ATN are seen in EXTRAHEPATIC manifestations of what hepatitis virus?

A

HAV

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23
Q

Pancreatitis, Myocarditis and Thyroiditis are EXTRAHEPATIC manifestations of what hepatitis virus?

A

HEV

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24
Q

In which VARIANT of viral hepatitis are the ALK PHOS and T.bilirubin HIGHLY ELEVATED with jaundice and can last up to 12 WEEKS?

A

CHOLESTATIC variant of HAV

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25
Q

In which VARIANT of viral hepatitis do the LFTs (ALT & Bili) normalize then RELAPSE every 4-15 WEEKS for up to a YEAR with POSITIVE IgM?

A

RELAPSING HAV

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26
Q

The ELEVATED LFTs which ocurr in acute HBV infection is associated with what?

A

POSITIVE SEROLOGIES (HBcAb IgM & IgG, HBsAg, HBeAg, HBV DNA)

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27
Q

HBsAb & HBeAb develop in what percentaage of the population signifying what?

A

>95% (spontaneous resolution of HBV - immune to re-infection)

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28
Q

Which patients typically develop HBV IMMUNE TOLERANT STATE?

A

Those who contracted the virus in INFANCY

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29
Q

Which SEROLOGIES remain POSITIVE in the HBV IMMUNE TOLERANT STATE (normal ALT, no inflammation, no fibrosis)?

A

HBV DNA (very HIGH)
HBsAg
HBeAg
HBcAb IgG

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30
Q

What is the TREATMENT of HBV IMMUNE TOLERANT STATE?

A

NONE

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31
Q

What is CHRONIC HBV (loss of immune tolerant stage)?

A

HBeAg POSITIVE

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32
Q

A patient with a DROP in HBV DNA, POSITIVE HBeAg, ELEVATED ALT from a state of HIGH HBV DNA with normal ALT indicates what?

A

Conversion to ACTIVE HBV infection and LOSS of IMMUNE TOLERANT STATE (50% of immune tolerant patients in 5 years)

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33
Q

What should be done with IMMUNE TOLERANT STATE patients?

A

MONITORED regularly for convesion to CHRONIC HBV and loss of immune tolerant state - 50% in 5 years (may develop the HBeAb)

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34
Q

Which Hep B patients in the IMMUNE TOLERANT (IT) phase should be TREATED?

A

Those at HIGH-RISK of LIVER CANCER (family history, ALT >25, age >45, significant inflammation or fibrosis on liver biopsy)

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35
Q

What is the DETERMINING FACTOR of whether a patient has ACTIVE or INACTIVE Hep B?

A

Presence or Absence of the HBeAg
If present (active) if HBeAb present (inactive)

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36
Q

What happens when CHRONIC Hep B patients have a FLARE (LFTs go up) in which HBeAg dissapears and HBeAb appears (HBsAg still present, HBcAb IgG present, HBcAb IgM may be positive again, HBV DNA decreases or disappears)?

A

Spontaneous loss of HBeAg with INACTIVE Hep B

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37
Q

What can happen if a Hep B patient FLARES (loss of HBeAg)?

A

Can develop Acute Liver Failure (ALF)

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38
Q

How can you have HBeAg NEGATIVE ACTIVE Hep B?

A

Mutation in the e-GENE of the HBV

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39
Q

Why is the eAg so important in Hep B?

A

Because it is the TARGET of the IMMUNE response to INACTIVATE Hep B (without it, HBV CANNOT be inactivated)

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40
Q

What is DIFFERENT about the CHOLESTATIC form of Hep A infection vs non-cholestatic form?

A

In the CHOLESTATIC form, Alk Phos is MUCH HIGHER

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41
Q

What remains POSITIVE in the RELAPSING form of Hep A?

A

Hep A IgM

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42
Q

In Hep B patients, what is significant about LOSS of HBsAg and gain of the HBsAb?

A

RESOLUTION of Hep B

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43
Q

WHY is the E-antigen PRESENCE important?

A

Because it is the TARGET of our IMMUNE response, without it, an e-Ag

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44
Q

What did the REVEAL study show?

A

That the risk of developing cirrhosis amd HCC from HBV was DIRECTLY related to HBV DNA levels

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45
Q

At what level of HBV DNA is the risk of developing HCC VERY HIGH?

A

> 20,000

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46
Q

At what HBV DNA level should you treat a patient with chronic diseases, comorbidities, >50 yo and HBeAg NEGATIVE status?

A

>2,000 (because RISK of HCC starts getting higher between 2,000-20,000)

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47
Q

In otherwise HEALTHY patients especially HBeAg POSITIVE, at what level of DNA would you start treatment?

A

> 20,000

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48
Q

What MUST be tested for ALL individuals who have Hep B whether active or inactive disease?

A

US every 6 MONTHS

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49
Q

In which hepatitis, HBV or HCV can you develop HCC WITH or WITHOUT cirrhosis?

A

HBV (in HCV, ONLY with cirrhosis)

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50
Q

Whom whould be vaccinated for Hep B?

A

ALL CHILDREN (and healthcare workers)

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51
Q

Whom should be vaccinated for Hep A?

A

ALL individuals prior to TRAVEL to endemic areas (Caribbean, Mexico)

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52
Q

In households of INTIMATE CONTACTS of individuals with HAV or HBV, how should they be treated?

A

Serum IgG or HBIG (Hep B IgG)

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53
Q

What individuals require a Hep B BOOSTER?

A

If initially vaccinated and responded (HBsAb+) and then when exposed, you had HBsAb- (years later), GET a BOOSTER and document HBsAb+ THAT’S IT, NO MORE boosters after further exposures

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54
Q

50% of Hep B GENOTYPE A patients SEROCONVERT (HBsAb/HBeAb) with what DRUG?

A

PEG-Interferon

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55
Q

In what HBV patients is PEG-INF NOT able to be used?

A

HBeAg NEGATIVE (only TDF, TAF-less drug, less toxic or Entecavir)

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56
Q

WHEN can you stop therapy in HBeAg NEGATIVE patients?

A

NEVER

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57
Q

WHEN can you STOP THERAPY in HBeAg POSITIVE patients?

A

6 MONTHS after they SEROCONVERT(HBeAb)

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58
Q

When initiating ANTIBIOLOGIC treatment for IBD in a patient positive for HBV an HCV what else do you do?

A

TREAT for BOTH HBV and HCV as well as the IBD (because HBV WILL FLARE even if inactive)

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59
Q

HBV patients with POSITIVE HBsAg treated with long-term IMMUNOTHERAPY, MONOCLONAL BIOLOGIC agents, CANCER CHEMOTHERAPY or treatment of CHRONIC HCV CO-INFECTION MUST BE TREATED for?

A

HBV with ANTIVIRAL agents

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60
Q

When using RITUXIMAB, if a patient is HBsAg NEGATIVE BUT HBcAb POSITIVE, or HBsAg NEGATIVE and HBsAb NEGATIVE or LOW-TITER HBsAb, they require treatment for?

A

HBV with ANTIVIRAL agents

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61
Q

In a patient with chronic HCV and Y93H mutation, how do you TREAT?

A

EPCLUSA (SOFosbuvir + VELpatasvir) for 12 WEEKS (DO NOT use in CIRRHOSIS with the Y93H mutation)

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62
Q

HCV patients with CHILDS CLASS B & C cannot use WHAT antiviral drugs in their treatment regimens?

A

PROTEASE INIBITORS (SOFosbuvir)

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63
Q

Which HCV patients are NOT treatment candidates?

A

LIMITED life expectancy and MILD fibrosis
ADVANCED stage 3-4 HCC
CHILDS Class C CIRRHOSIS with HIGH MELD who ARE TRANSPLANT candidates
ACTIVE IVDA who don’t want to stop

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64
Q

What do you use to SCREEN ALL patients for HBV who will begin treatment for HCV?

A

ALL 3 MARKERS: HBsAg, HBcAb, HBsAb

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65
Q

Patient has ACTIVE HBV and is about to begin treatment for HCV, how do you treat?

A

BOTH HBV and HCV therapy

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66
Q

Patient has INACTIVE HBV and is about to begin treatment for HCV, how do you treat?

A

Treat HCV and HBV (prophylaxis) then STOP HBV treatment 6 MONTHS after HCV is cured

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67
Q

Patient has ISOLATED HBcAb and is about to begin treatment for HCV, how do you treat?

A

ONLY the HCV, monitor for HBV

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68
Q

Patient has RESOLVED HBV (HBsAb) and is about to begin treatment for HCV, how do you treat?

A

ONLY HCV

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69
Q

If a patient is POSITIVE for HBsAg, what do you test for next?

A

HBV DNA;
HBeAg;
HBeAb

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70
Q

What happens to the LIVER of patients who are successfully treated for HBV and HCV?

A

Regression of FIBROSIS and CIRRHOSIS

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71
Q

Curing patients of HCV reduces their RISK of developing what THREE associated DISEASES?

A

B-Cell Lymphoma; DM, ESRD

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72
Q

Does CHRONIC LIVER DISEASE or CIRRHOSIS increase the risk of drug-induced hepatotoxicity?

A

NO

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73
Q

What happens if DRUG TOXICITY occurs in a patient with CIRRHOSIS or CHRONIC LIVER DISEASE?

A

It will be MORE SEVERE and increase the risk of developing ALF

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74
Q

What are the two most common agents of DILI in CHILDREN?

A

ASA, VALPROIC ACID

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75
Q

What factors increase the risk for DILI in adults?

A

Age >50, Obese, Malnourished, Women, Dose, Alcohol

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76
Q

Hepatic Phase I (cyt P450) does what to an ingested drug that makes it potentially toxic or an allergen (fever, rash, eosinophilia)?

A

Makes it into an ACTIVE METABOLITE

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77
Q

What is the hepatic Phase II reaction of an ingested drug?

A

DETOXIFIES active metabolites and makes them into waste products

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78
Q

What GENETIC mechanism results in PRESENCE or ABSENCE of TOXICITY to INH?

A

Genetic variation in ACETYLATING enzymes (fast/slow) in individuals

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79
Q

What do cyt P450 competitor drugs cause?

A

REDUCTION of active metabolite (toxic or not)

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80
Q

What do cyt P450 INDUCER drugs cause?

A

INCREASE of active metabolite (toxic or not)

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81
Q

What happens when two or more drugs COMPETE for cyt P450?

A

ACTIVE (potentially toxic) metabolites get created more SLOWLY, hence LESS active drug and less TOXICITY

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82
Q

Which are the FOUR (4) most common cyt P450 INDUCERS (cause active metabolite to be created whether toxic or not)

A

ETHANOL, PHENYTOIN, RIFAMPIN, OMEPRAZOLE

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83
Q

What is the HEPATIC process of ADAPTATION?

A

Initial LFT ELEVATION with a drug (up to 3x NL) then the LFTs normalize

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84
Q

If a patient does not undergo hepatic ADAPTATION with a new drug, what could be the UNDERLYING cause?

A

NAFLD

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85
Q

In a patient whom was started on a drug and LFTs are in the 3-5 x ULN, what is the next step?

A

If NO JAUNDICE, monitor. If develops jaundice STOP (10% risk of ALF)

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86
Q

In a patient started on a drug, LFTs are in the 3-5 x ULN and they develop JAUNDICE, or if the LFTs are 5 x ULN, what is the next step?

A

STOP the drug, give N-acetylcysteine

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87
Q

In a patient taking a new DRUG, with LFT elevation, what do you do if JAUNDICE occurs?

A

Immediately STOP the drug

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88
Q

What is the most COMMON type of DILI, it resolves when the drug is STOPPED, there is JAUNDICE and ITCHING?

A

CHOLESTATIC (elevated ALK PHOS and BILIRUBIN rather than ALT/AST) jaundice is NOT an ominous sign as with non-cholestatic DILI

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89
Q

In a patient whom received CHEMOTHERAPY in the past, what is the most common HEPATIC presentation?

A

ASCITES

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90
Q

THROMBOSIS of which HEPATIC vessel causes ASCITES?

A

HEPATIC VEIN (not portal vein) - becauses it causes NON-CIRRHOTIC PORTAL HTN

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91
Q

What is SINUSOIDAL OBSTRUCTIVE SYNDROME (SOS)?

A

Chemotherapy-induced liver injury with PORTAL HTN, ASCITES, VARICES but NORMAL-APPEARING LIVER on imaging

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92
Q

Besides sinusoidal obstructive syndrome, what is the other liver INJURY that CHEMOTHERAPY can cause?

A

NODULAR REGENERATIVE HYPERPLASIA vascular injury to the portal tracts (hepatocytes proliferate between fortal tracks WITHOUT cirrhosis) - liver LOOKS NODULAR

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93
Q

What type of IMMUNOTHERAPY causes HEPATOTOXICITY in ~60 DAYS after starting drug, AST/ALT elevated (600) and ALP (300)? How is it TREATED?

A

Check Point Inhibitors (CHI)
Treat with STEROIDS +/- Mycophenolate Mofetil or STOP DRUG

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94
Q

If a patient develops HEPATOTOXICITY with Check Point Inhibitors, what is their RISK of developing this again with RE-TREATMENT?

A

17%-28%

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95
Q

What is meant by an acetaminophen THERAPEUTIC MISADVENTURE?

A

When an acetaminophen OVERDOSE is caused by a LOWER THAN NORMAL toxic dose taken in COMBINATION with other cyt P450 INDUCERS like ALCOHOL

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96
Q

What INCREASES RISK of HEPATOTOXICITY with ACETAMINOPHEN in patients with CHRONIC LIVER DISEASE or CIRRHOSIS?

A

Drinking ALCOHOL in past 6 MONTHS

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97
Q

How LATE post ACETAMINOPHEN TOXICITY is N-ACETYLCYSTEINE still 100% EFFECTIVE?

A

Up to 16 HOURS (16-24 hours 3% mortality, >24 hours 15% mortality)

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98
Q

If a patient presents with ACETAMINOPHEN TOXICITY >24 HOURS, how do you TREAT?

A

IMMEDIATE N-ACETYLCYSTEINE and TRANSFER to TRANSPLANT center

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99
Q

STEROIDS are ONLY effective treatment for what LIVER DISEASES?

A

AIH (includes checkpoint inhibitors)
ACUTE ALCOHOLIC HEPATITIS

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100
Q

Which SEROLOGIC markers are relevant to AIH, PBC and PSC?

A

AIH: ANA, SMA
PBC: AMA
PSC: ANCA

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101
Q

What are the BIOCHEMICAL patterns seen in AIH, PBC and PSC?

A

AIH: Hepatocellular (AST/ALT)
PBC: Cholestatic (ALP/Bili)
PSC: Cholestatic/Mixed

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102
Q

What is the HISTOLOGY pattern seen in AIH, PBC and PSC?

A

AIH: Piecemeal Necrosis, Lobular Inflammation, Interface hepatitis
PBC: Inflammatory Cholangiopathy
PSC: Bland Portal and Periductal FIBROSIS

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103
Q

Which of AIH, PBC, PSC is seen predominantly in MEN?

A

PSC

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104
Q

Which of AIH, PBC, PSC is associated with HLA DR3/DR4?

A

AIH

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105
Q

Which of AIH, PBC, PSC is associated with HLA DRW8?

A

PBC

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106
Q

Which of AIH, PBC, PSC is associated with HLA B8/DR3?

A

PSC

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107
Q

Sicca Syndrome, RA and Thyroid disease are AI disorders seen in which autoimmune liver disease?

A

PBC

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108
Q

IBD (80% UC) is associated with which autoimmune liver disease?

A

PSC

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109
Q

What are the positive SEROLOGIC markers seen in AIH Type-I?

A

ANA, SMA

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110
Q

A more SEVERE and RAPIDLY PROGRESSIVE form of AIH found in EUROPEANS, Type-II has which SEROLOGIC markers?

A

Anti-LKM (liver, kidney, microsomal)
Anti-LC1

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111
Q

PERSISTENT ALT/AST elevation, abnormal liver US, abnormal ELASTOGRAPHY but NEGATIVE SEROLOGIC markers? Next step?

A

AIH - ALWAYS BIOPSY before treating

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112
Q

What is OFTEN confused for NASH prior to BIOPSY based on ALT/AST and imaging?

A

AIH

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113
Q

A patient found with STABLE or DECOMPENSATED cirrhosis with NORMAL LFTs, NO INFLAMMATION on liver biopsy, and positive SEROLOGIC markers for AIH? How do you TREAT?

A

CRYPTOGENIC (burned-out) CIRRHOSIS
NO TREATMENT (no improvement)

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114
Q

What do you do for a patient with AIH who develops hepatic DECOMPENSATION?

A

Liver TRANSPLANT

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115
Q

How LONG do you treat AIH with PREDNISONE for? Then?

A

Until ALT is NORMAL (start at 60, HOLD at 20)
Once ALT is normal KEEP at 5-10 mg DAILY for a YEAR
Then ADD Immunologic (azathioprine, MMF, etc.)

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116
Q

Can AIH be treated ONLY with PREDNISONE then taper to OFF?

A

NO, must add bilologic (azathioprine, MMF, etc.)

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117
Q

How LONG do you treat AIH with prednisone + azathioprine prior to DISCONTINUING prednisone?

A

12-24 MONTHS

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118
Q

When AIH treatment RELAPSE occurs, what DOSE of prednisone do you RESTART?

A

20 mg

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119
Q

What can you SUBSTITUTE for PREDNISONE when treating AIH if patient is intolerant?

A

BUDESONIDE

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120
Q

If patient with AIH is intolerant to azathioprine, what else can you use?

A

Mycophenolate Mofetil or Cyclosporine or Tacrolimus

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121
Q

In a patient treated for AIH whose ALT does NOT NORMALIZE by 6 MONTHS, what do you do?

A

CHANGE treatement (budesonide, MMF, cyclosporine, tacrolimus) or consider alternative diagnosis

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122
Q

How do you treat MILD to MODERATE AIH (very mild ALT elevation and very MILD to NO INFLAMATION on BIOPSY)?

A

MONITORING of ALT, FIBROSCAN and RE-BIOPSY as needed

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122
Q

Once PREDNISONE or budesonide is STOPPED for a patient with AIH, how LONG do you continue IMMUNOTHERAPY and MONITORING (azathioprine, etc)?

A

LIFE-LONG (80% will relaspe if stopped)

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123
Q

WHAT will you see on liver BIOPSY in 33% of AIH patients in spite of NORMAL ALT and on immunosuppressive therapy?

A

Progression of FIBROSIS

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124
Q

Sarcoidosis, Amyloidosis, TB, Lymphoma, SCC, Fungal infections all casue what type of LIVER DISORDER?

A

INTRAHEPATIC CHOLESTASIS (elevated ALP) - these must be BIOPSIED as well

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125
Q

Which AMA assay is done by most labs (for PBC)?

A

M2 (directed against the pyruvate dehydrogenase of the inner mitochondrial membrane)

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126
Q

These symptoms require LIVER TRANSPLANTATION intractable PRURITUS, JAUNDICE, ASCITES, VARICEAL BLEEDING, HE and are found in?

A

PBC

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127
Q

What is the TREATMENT of PBC (to normal ALP)? If treating for months and ALP is lower but still not normal?

A

URSO (ursodeoxycholic acid 15 mg/kg) - reduces toxicity of bile
Obeticholic acid (5 mg and increase to 10 mg depending on response)

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128
Q

In patients with PBC, what SEROLOGY determines risk of MORTALITY (or need for liver TRANSPLANT)?

A

ALP (and biliruibin)

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129
Q

Patients >50 yo treated for PBC with URSO long term require MONITORING for what?

A

OSTEOPOROSIS (DEXA scan) - start CALCIUM + VIT D if diagnosed or consider ESTROGEN if postmenopausal
If DECREASED bone density but not osteoporosis, start DIPHOSPHONATE
Also DENTAL CARIES

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130
Q

PBC can also cause HYPERCHOLESTEROLEMIA (xantolasmas) why does this NOT cause CAD and why is it NOT TREATED?

A

Because it is HDL that is ELEVATED

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131
Q

STRICTURES & BEADING in large to medium size BILE DUCTS, MRCP is diagnostic?

A

LARGE-DUCT PSC (biopsy is ONLY needed for staging, prefer FIBROSCAN)

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132
Q

ALP elevated, with NORMAL AST/ALT, NORMAL CHOLANGIOGRAM, need BIOPSY for DIAGNOSIS?

A

SMALL-DUCT PSC (can use URSO but NO defined treatment for SMALL DUCT ONLY - if no drop in ALP, can stop)

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133
Q

What indicates future need for TRANSPLANTATION in patient with PSC (for which there is no treatment)?

A

SYMPTOMATIC disease (jaundice)

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134
Q

What is the MEAN survival time in YEARS from DIAGNOSIS to CIRRHOSIS (needing transplantation) for patients with PSC?

A

20 years

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135
Q

WHEN is the ONLY time PSC patients require ENDOSCOPIC management (ERCP) ? NO EFFECT ON SURVIVAL

A

When they develop SYMPTOMATIC PERSISTENT JAUNDICE or develop CHOLANGITIS due to BILIARY SEPSIS due to HIGH-GRADE CBD STRICTURES

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136
Q

What are the RISKS of ERCP in PSC patients who do NOT have symptomatic CBD strictures (persistent jaundice, cholangitis)?

A

CHRONIC cholangitis, liver ABSCESS, acelerated need for liver TRANSPLANT

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137
Q

What is the ONLY TRIAL drug that shows promise in PSC?

A

CILOFEXOR (decreased ALP)

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138
Q

What is the single greatest RISK factor for CHOLANGIOCARCINOMA (progressive jaundice and weight loss)?

A

PSC (check CA19-9 and CEA)

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139
Q

What are the ONLY tests useful for SCREENING for CHOLANGIOCARCINOMA?

A

CT or MRCP every 6-12 MONTHS, CA19-9, CEA

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140
Q

In a patient with STRONG suspicion for PSC with NORMAL imaging, what do you treat for?

A

SMALL-DUCT PSC

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141
Q

If LFTs are OFF (as in OVERLAP syndromes) what do you use as guide for TREATMENT?

A

SEROLOGIES and HISTOLOGY

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142
Q

Elevated IgG4, biopsy with INFLAMMATION and FIBROSIS (pancreas, bile ducts, LNs, salivary glands, retroperitoneum) and if biliary, elevated LFTs with biliary strictures?

A

IgG4-ASSOCIATED CHOLANGITIS

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143
Q

How is IgG4-ASSOCIATED CHOLANGITIS treated?

A

PREDNISONE + MMF or RITUXIMAB

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144
Q

IgG4 or SAUSAGE-LIKE biliary dilation, elevated LFTs, INFLAMMATORY masses in PANCREAS or LNs or BILE DUCTS or SALIVARY glands or RETROPERITONEUM?

A

IgG4-ASSOCIATED CHOLANGITIS

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145
Q

What should you ALWAYS check for in a patient with PSC and why?

A

IgG4-ASSOCIATED CHOLANGITIS (because its TREATABLE)

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146
Q

Decreased serum ALBUMIN, increased CHOLESTASIS and TELANGIECTASIAS (spider angiomas, palmar erythema, small varices) are all NORMAL during this process?

A

PREGNANCY

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147
Q

Are chnages in AST/ALT, GGT, PT or BILIRUBIN normally expected in PREGNANCY?

A

NO

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148
Q

What is the safest time during PREGNANCY to have SURGERY or an ERCP for gallstones, etc.?

A

2nd Trimester

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149
Q

In a PREGNANT patient, when traveling ABROAD, what VIRUS affords the highest RISK of FULMINANT HEPATIC FAILURE?

A

Hep E

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150
Q

Are treatments such as INF and RIBAVIRIN ok to use in PREGNANCY to treat Hep E?

A

NO

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151
Q

This hepatitis VIRUS is associated with PRE-TERM labor and premature RUPTURE of MEMBRANES and IgG MUST be given to neonate if infection occurs within 2 WEEKS of pregnancy?

A

Hep A

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152
Q

Having this VIRUS can cause SEVERE HEPATITIS (74% mortality) in the 2nd/3rd TRIMESTER with VERY HIGH LFTs, present with FEVER and UPPER RESPIRATORY INFECTION, NO JAUNDICE with near-normal bilirubin?

A

HSV

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153
Q

What is seen on LIVER BIOPSY in patients with HSV hepatitis (pregnant women in 2nd/3rd trimester)?

A

Patchy NECROSIS and VIRAL INCLUSION BODIES

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154
Q

What is the ONLY acceptable wat to DIAGNOSE HSV HEPATITIS in pregnancy and how do you TREAT?

A

Diagnose: HSV PRC
Treat: ACYCLOVIR (can suspect, don’t need to have diagnosis)

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155
Q

What hepatitis VIRUSES should be screened for in ALL PREGNANT women?

A

HBV/HCV

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156
Q

What FACTOR determines RISK of TRANSMISSION of HBV from mother to CHILD?

A

HBV DNA

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157
Q

Besides DNA VIRAL LOAD, what THREE FACTORS INCREASE the risk of TRANSMISSION of HBV from pregnant mother to CHILD?

A
  1. Presence of HBeAg (90%)
  2. Anti-partum HEMORRHAGE
  3. MECONIUM-stained amniotic fluid
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158
Q

At what HBV VIRAL DNA LOAD should a pregnant woman in her 3rd TRMIESTER be given PROPHYLAXIS (TENOFOVIR) to prevent vertical TRANSMISSION?

A

> 2 x 10^5 (>200,000 copies)

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159
Q

What medical PROCEDURES whould be AVOIDED for a PREGNANT patient with HBV or HCV?

A

AMNIOCENTESIS, INVASIVE fetal monitoring or EPISIOTOMY

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160
Q

Is a C-Section recommended over vaginal delivery for PREGNANT mothers with HBV?

A

NO

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161
Q

Is it OK to BREASTFEED for a woman with HBV?

A

YES (HBV is NOT found in breast milk)

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162
Q

What is the TREATMENT of a PREGNANT mother with HBV (viral load >200,000 and HBeAg+) and CHILD?

A

Mother: TDF (not TAF) a 28-32 WEEKS
Child: HBV IgG at BIRTH, VACCINE within 12 hrs, MONTH 1 and MONTH 6

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163
Q

What is the TREATMENT of a PREGNANT mother with HBV (viral load < 200,000 and HBeAg-) or PRE-TERM and CHILD?

A

Mother: NOTHING
Child: HBV IgG at BIRTH, VACCINE within 12 hrs, MONTH 1 and MONTH 6

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164
Q

Can HCV VERTICAL TRANSMISSION be PREVENTED?

A

NO NOT even by C-Section (but low, 3-10%)

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165
Q

What CO-INFECTION with HCV makes VERTICAL TRANSMISSION higher RISK in PREGNANT women?

A

HIV (11-19%)

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166
Q

WHEN do you TEST an infant for HCV if born to a POSITIVE mother?

A

On TWO occasions between 2-6 MONTHS
And/Or AFTER 18 MONTHS

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167
Q

WHEN is BREASTFEEDING ok for a mother with HCV?

A

If no NIPPLE TRAUMA and no HIV CO-INFECTION

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168
Q

With which hepatitis VIRUS can you see POST-PARTUM FLARES?

A

HBV

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169
Q

PREGNANT women have a 20X increased RISK of INTRAHEPATIC CHOLESTASIS of PREGNANCY if infected with which VIRUS?

A

HCV

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170
Q

Why should PREGNANT women have their HCV status re-evaluated POSTPARTUM?

A

Because 10% SPONTANEOUSLY clear the virus

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171
Q

WHEN should a HCV positive WOMAN who wants children be treated for HCV?

A

BEFORE CONCEPTION or AFTER DELIVERY
If wants to breastfeed, AFTER done BREASTFEEDING

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172
Q

How LONG should a woman WAIT to become PREGNANT and MUST use DUAL CONTRACEPTION after LAST DOSE of RIBAVIRIN (TERATOGEN)?

A

6 MONTHS

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173
Q

What is the ONLY SAFE treatment of AIH in PREGNANCY?

A

PREDNISONE + AZATHIOPRINE (cannot use MMF, etc.)

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174
Q

What are the risks to PREGNANCY with AIH?

A

PREMATURITY and FETAL LOSS

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175
Q

What can happen to AIH with PREGNANCY?

A

FLARE (monitor LFTs but LIMIT CHANGING therapy) INTRAPARTUM and POSTPARTUM (check every 2-4 weeks for 6 months)

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176
Q

What needs to CHANGED about treating WILSON’s DISEASE in pregnancy if treating with chelation therapy with D-Penicillamine or TRIENTENE?

A

REDUCE dose in 3rd TRIMESTER by 25-50%

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177
Q

What needs to SUPPLEMENTED when treating WILSON’s DISEASE in pregnancy with chelation therapy with TRIENTENE?

A

IRON (chelates IRON besides copper)

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178
Q

Can a woman BREASTFEED if being treted for WILSON’s DISEASE with CHELATION therapy (D-Peniciliamine or Trientene)?

A

NO (causes copper deficiency to child)

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179
Q

Hepatocellular Adenomas (HCA) >5 cm in size are at an increased RISK for what in PREGNANCY and WHY?

A

RUPTURE with HEMORRHAGE
ESTROGEN DEPENDENT

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180
Q

If BEFORE PREGNANCY a hepatocelluar adenoma is found to be < 5 cm, what needs to be DONE?

A

MONITOR every TIMESTER and 12 WEEKS POSTPARTUM

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181
Q

If a hepatocelluar adenoma is found to be >5 cm BEFORE PREGNANCY, what can be done?

A

EMBOLIZATION or RESECTION

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182
Q

If a hepatocellular adenoma BECOMES >5 cm DURING PREGANANCY, what is done?

A

Bland EMBOLIZATION

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183
Q

A patient presents at 30 weeks gestation with intense pruritus, her ALT/AST ALP and T.bili are all elevated. US shows no gallstones of duct dilation, what’s the NEXT step for THIS diagnosis?

A

Measure SERUM BILE ACID LEVELS
Intrahepatic Cholestasis of Pregnancy

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184
Q

How do you TREAT hyperemesis gravidarum (1-20 weeks of pregnancy)?

A

IVFs, Vit B6, Antiemetics (ondansetron, promethazine, metoclopramide)

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185
Q

How do you TREAT Intrahepatic Cholestasis of Pregnancy (2nd and 3rd trimesters)?

A

URSO 15 mg/kg
EARLY DELIVERY (37 weeks)

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186
Q

How do you TREAT ACUTE FATTY LIVER OF PREGNANCY (3rd trimester)?

A

PROMPT DELIVERY (monitor infant for LCHAD deficiency)

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187
Q

ECLAMPSIA, PRE-EXCLAMPSIA and HELLP syndromes occur at 20-22 weeks of pregnancy, what is PARAMOUNT to treatment?

A

IMMEDIATE DELIVERY (if after 34-36 weeks)

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188
Q

Besides prompt DELIVERY (after 34-36 weeks) for a patient with HELLP, what ELSE must you TREAT the mother with?

A

PLATELET TRANSFUSION to 40K-50K platelets

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189
Q

Nulliparity, DM, OBESITY, HYPOthyroidism, TWIN pregnancy are all RISK factors for what PRENGNANCY-associated syndrome?

A

HYPEREMESIS GRAVIDARUM (elevated LFTs, unconjugated bilirubin)

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190
Q

What PREGNANCY SYDROME are Scandinavians and Chilean Indians more prone to?

A

Intrahepatic Cholestasis of Pregnancy

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191
Q

PREGNANT woman with persistent PRURITUS (palms and soles, nocturnal), BILE ACIDS >10 mmol/L?

A

Intrahepatic Cholestasis of Pregnancy

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192
Q

What are the TWO most common DEFICIENCIES noted in women who develop intrahepatic cholestasis of pregnancy?

A

Vit D & SELENIUM

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193
Q

Elevated maternal AGE, history of CHOLESTASIS with OCPs, CHRONIC HCV (20 X the risk) or FAMILY HISTORY of this condition are the RISK factors for?

A

Intrahepatic Cholestasis of Pregnancy

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194
Q

What special TESTING is recommended in a patient with RECURRENT Intrahepatic Cholestasis of Pregnancy, early onset of this or severe case with bile acids >100 mmol/L?

A

GENETIC TESTING

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195
Q

This condition usually occurs in the 2nd-3rd trimester (25-32 weeks) with PRURITUS of the PALMS and SOLES at night, STEATORRHEA, ELEVATED ALP, mild GGT elevation, HIGHLY ELEVATED BILE ACIDS (10-100 ULN), ELEVATED LFTs and MILD BILIRUBIN elevation?

A

Intrahepatic Cholestasis of Pregnancy

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196
Q

What SEROLOGIC factor is the KEY to diagnosis of Intrahepatic Cholestasis of Pregnancy?

A

ELEVATED BILE ACIDS

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197
Q

What is the TREATMENT for Intrahepatic Cholestasis of Pregnancy?

A

URSO, Vit K, Delivery at 37 WEEKS

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198
Q

Can Intrahepatc Cholestasis of Pregnancy RECCUR with subsequent pregnancies?

A

YES (65%)

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199
Q

Pregnant woman presents with HTN, SUDDEN WEIGHT GAIN, BLURRY VISION, EDEMA, PROTEINURIA (>300 mg/24h), ELEVATED LFTs?

A

PREECLAMPSIA/ECLAMPSIA

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200
Q

Nulliparity, maternal Age >40, FH, Chronic HTN, CKD, DM are all RISK factors forthis condition which can result in liver HEMATOMAS, RUPTURE (sudden onset abdominal pain with radiation to shoulder, shock, fever)?

A

PREECLAMPSIA/ECLAMPSIA

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201
Q

When do you DELIVER a patient with PREECLAMPSIA/ECLAMPSIA

A

34 WEEKS

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202
Q

If a PREGNANT woman presents with symptoms of HEMOLYSIS, elevated LFTs and LOW PLATELETS, when do you DELIVER?

A

ASAP (especially if >34 weeks)

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203
Q

WHEN can HELLP syndrome occur?

A

2nd-3rd trimester (28-36 weeks)
and up to 1 WEEK POSTPARTUM

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204
Q

In a PREGNANT woman with HIGH LFTs (AST/ALT >1,000) with ABDOMINAL PAIN RADIATING TO SHOULDER? NEXT STEP?

A

HEPATIC INFARCTION, SUBCAPSULAR BLEED or RUPTURE
CALL SURGERY or IR, CORRECT COAGULOPATHY

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205
Q

HOW do you treat PREGNANT woman with HELLP at DELIVERY or for PROCEDURES?

A

TRANSFUSE PLATELETS to >40K

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206
Q

This condition typically ocurs during the THIRD trimester (around week 36) as well as POST PARTUM with MICROVESICULAR FATTY LIVER (not well seen on US) especially with HOMOZYGOUS LCHAD babies (spill and accumulate in liver)?

A

ACUTE FATTY LIVER of PREGNANCY

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207
Q

Pregnant woman at 36 WEEKS gestatio presents with ENCEPHALOPATHY, elevated LFTs, HYPOglycemia, LEUKOCYTOSIS, ASCITES, elevated Cr, COAGULOPATHY? TREAT?

A

AFLP (acute fatty liver of pregnancy)
DELIVER and SUPPORTIVE therapy for liver (may need TRANSPLANT if does not improve)

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208
Q

What is the SAFEST CONTRACEPTIVE for women with CHRONIC LIVER DISEASE (besides condom)?

A

IUD

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209
Q

Women with chronic liver disease with THROMBOSIS, ADENOMAS, decompensated CIRRHOSIS and NAFLD should AVOID which contraceptives?

A

COMBINED HORMONAL CONTRACEPTIVES

210
Q

Do women with CHRONIC LIVER DISEASE have DIFFICULTY with REPRODUCTION?

A

YES

211
Q

Is ASSISTED REPRODUCTION SAFE in women with CIRRHOSIS?

A

ONLY CHILD’s A (bilirubin, albumin, INR, ascites)

212
Q

Is REPORDUCTION affected in MEN with chronic liver disease?

A

YES (feminization, low testosterone, elevated estrogen with ED, testicular atrophy, oligospermia)

213
Q

Women with CIRRHOSIS (compensated or not) who become PREGNANT, are a HIGH-RISK of what on US?

A

SPLENIC ARTERY ANEURYSM wich can rupture especially if >2 cm (due to INCREASED portal HTN)

214
Q

In women with CHRONIC LIVER DISEASE, the PHYSIOLOGIC changes of PREGNANCY cause what?

A

INCREASED PORTAL HTN (ascites, varices, HE)

215
Q

In women with CIRRHOSIS, if become PREGNANT, most complications will occur because of what condition?

A

PORTAL HTN (splenic artery aneurysm, bleeding varices, ascites)

216
Q

In a woman who is CIRRHOTIC and PREGNANT with PORTAL HTN, the risk of RUPTURE of a SPLENIC ARTERY ANEURYSM is VERY HIGH if how LARGE?

A

>2 cm

217
Q

What is the RECOMMENDATION for a woman with CIRRHOSIS who has had VARICEAL SURVEILLANCE within 1 YEAR PRIOR to conception and had SMALL to LARGE varices?

A

Non-selective beta blocker or EGD with BANDING

218
Q

What is the RECOMMENDATION for a woman with CIRRHOSIS who has NOT had VARICEAL SURVEILLANCE PRIOR to conception and has SMALL to LARGE varices?

A

SECOND TRIMESTER ONLY: non-selective beta blocker or EGD with BANDING

219
Q

Which non-selective BETA BLOCKER do you use for PREGNANT women who have VARICES?

A

PROPRANOLOL (NOT nadolol)

220
Q

In PREGNANT women with CIRRHOSIS, what is a PREDICTOR of COMPLICATIONS (most occur 2nd-3rd trimester)?

A

MELD >10

221
Q

In PREGNANT women whom received a liver TRANSPLANT, what are two commonly seen ISSUES?

A

GESTATIONAL DIABETES
HYPERTENSIVE disorders

222
Q

In PREGNANT women whom received a liver TRANSPLANT there is a HIGH RISK of REJECTION if conception occurs WHEN?

A

WITHIN 6 MONTHS of TRANSPLANT

223
Q

In a CIRRHOTIC PREGNANT woman with ACTIVELY BLEEDING varices, what MEDS are OK to use?

A

OCTREOTIDE and CEPHALOSPORINS (prophylaxis) - do NOT use vasopressin or terlipressin

224
Q

In women whom received a liver TRANSPLANT, WHEN should CONCEPTION be ATTEMPTED?

A

ONE (1) YEAR post TRANSPLANT
or ONE (1) YEAR post REJECTION episode

225
Q

In women whom received a liver TRANSPLANT, which CONTRACEPTIVES are SAFE?

A

PROGESTERONE or IUDs (estrogen increases risk of thromboembolism and HTN)

226
Q

In women whom received a liver TRANSPLANT, and are thinking of PREGNANCY, what is IMPERATIVE?

A

CONTRACEPTION and PRECONCEPTION COUNSELING

227
Q

Which IMMUNOSUPRESSION drugs are OK to use (liver transplant, etc.) during PREGNANCY and how often do you monitor labs for LEVELS?

A

Tacrolimus, Cyclosporine, Azathioprine, Prednisone
(NEVER use mycophenolate mofetil, sirolimus/everolimus)
Monitor LEVELS every 2-4 weeks because levels will decrease with increased blood volume

228
Q

How LONG after using Mycophenolate Mofetil is it OK for BOTH MEN & WOMEN to plan PREGNANCY (BLACK BOX WARNING)?

A

6 MONTHS

229
Q

Can you BREASTFEED if on Mycophenolate Mofetil, EVEROLIMUS or SIROLIMUS?

A

NO

230
Q

Which IMAGING studies are helpful for CHOLESTATIC LIVER DISEASES?

A

US or MRPC

231
Q

Fatty liver infiltration with LOBULAR INFLAMMATION, CYTOLOGIC BALOONING, +/- MALLORY BODIES, +/- FIBROSIS?

A

STEATOHEPATITIS

232
Q

What TYPE of STEATOSIS do PREDNISONE, ALCOHOL and METABOLIC SYNDROME cause?

A

MACROvesicular steatosis

233
Q

WILSON disease, TPN, ESTROGEN, AMIODARONE, METHOTREXATE, TAMOXIFEN, HCV, PCOS, CELIAC disease, OSA, HYPO/HYPERthyroidism and post WHIPPLE procedure all cause what TYPE of STEATOSIS?

A

MACROvesicular

234
Q

VALPROIC ACID, HIV-DRUGS, AFLP and HELLP syndrome, LIPOSOMAL ACID LIPASE deficiency all cause this TYPE of STEATOSIS?

A

MICROvesicular

235
Q

What is the RISK of progressing to HCC in patients with CIRRHOSIS?

A

10%

236
Q

Female gender, obesity, viral hepatitis, Iron overload, smoking are all RISK factors for INCREASED LIVER INJURY with this activity?

A

Drinking ALCOHOL

237
Q

What is known to be PROTECTIVE against LIVER INJURY in those who drink ALCOHOL?

A

COFFEE

238
Q

Besides spider angiomas, what is another PHYSICAL sign of CHRONIC LIVER DISEASE?

A

DUPUYTREN CONTRACTURE

239
Q

LEUKOCYTOSIS (RULE OUT INFECTION) and an AST:ALT ratio of WHAT, is seen with ALCOHOLIC HEPATITIS?

A

1:2

240
Q

ALCOHOLIC HEPATITIS will RARELY present ALONE with LFTs >?

A

350 (look for concomitant disease)

241
Q

Besides alcohol cessation, what is one of the MOST IMPORTANT treatments of a patient with ALCOHOLIC HEPATITIS?

A

HIGH-PROTEIN NUTRITION (1.5 g/kg/day) with ~3,000 calories/day

242
Q

What VITAMINS and MINERALS must be SUPPLEMENTED in patients with ALCOHOLIC HEPATITIS?

A

Vit K, Thiamine (prevent Wernicke’s), Glucose, Folate, Mg, Phos, Potassium (may have elevated INR), Zinc

243
Q

What is the EQUATION for Maddrey’s discriminant function?

A

4.6 x (PT-control) + T.Bili
If >32, start steroids +/- NAC
Can use MELD, and if >20, start steroids +/- NAC

244
Q

This SCORE stratifies patients ALREADY RECEIVING steroids for ALCOHOLIC HEPATITIS for 7 days and predicts which will improve and which need other management?

A

Lille Score
< 0.45 - RESPONDING (85% 6 month survival)
> 0.45 - NOT RESPONDING (25% 6 month survival)

245
Q

In a patient with a FIRST EVENT, good SUPPORT system, INSIGHT into alcohol use disorder, no ILLICIT substance use, no prior FAILED REHAB, who presents with ALCOHOLIC HEPATITIS with Lille Score >0.45, what is the NEXT STEP?

A

TRANSFER to liver TRANSPLANT center

246
Q

When the DIAGNOSIS of ALCOHOLIC HEPATITIS is POSSIBLE (could be alpha-1 antitrypsin, UGIB, HTN, cocaine - 7 days, DILI - 30 days, atypical lab tests) but NOT PROBABLE, what should you do?

A

Liver BIOPSY

247
Q

Onset of JAUNDICE within PAST 8 WEEKS, ongoing ALCOHOL consumption for >6 MONTHS with < 60 days abstinence, AST/ALT both < 400, AST:ALT 1:2 and T.bili >3, what is this?

A

Alcoholic Hepatitis

248
Q

HOW do you check ALCOHOLIC HEPATITIS patients for INFECTION?

A

Blood, Urine, Ascites

249
Q

Is PENTOXIFYLINE still used to treat appropriate (high MDF score) alcoholic hepatitis patients?

A

NO (only steroids) - PREDNISONE 40 mg/day for 28 days +/- NAC - check LILLE score in 5-7 days

250
Q

Uncontrolled INFECTIONS, AKI Cr >2.5, uncontrolled GIB, HBV, HCV, HIV, HCC, DILI, TB and ACUTE PANCREATITIS, SHOCK, MULTIORGAN FAILURE are all CONTRAINDICATIONS to using which treatment for ALCOHOLIC HEPAITITS?

A

STEROIDS (consider TRANSPLANT)

251
Q

What TWO tests are available to check if a patient has CHRONICITY to their ALCOHOLIC HEPATITIS and not ACUTE?

A

Ethyl Glucoronide
Phosphatidylethanol

252
Q

Which mediations HELP with REHAB of ALCOHOLIC HEPATITIS?

A

NALTREXONE, DISULFIRAM, acamprosate, baclofen

253
Q

At what MELD-Na score should you REFER a patient to a liver TRANSPLANT center?

A

MELD-Na >21

254
Q

This disease is diagnosed by EXCLUSION, serum FERRITIN is mildly elevated < 1.5 x ULN (but not transferrin), ANA < 1:160, AMA < 1:40?

A

NAFLD

255
Q

Elevation in FERRITIN, TRANSFERRIN and IRON SATURATION, how to dignose?

A

Liver BIOPSY (hemochromatosis)

256
Q

If there is CONFUSION between AUTOIMMUNE LIVER DISEASE and NAFLD, what should you do?

A

Liver BIOPSY

257
Q

What is the natural PROGRESSION of NAFLD?

A

NAFLD (20%) to NASH (25%) to CIRRHOSIS (10%)

258
Q

What finding in LIVER INJURY predicts need for TRANSPLANT or risk of DEATH?

A

FIBROSIS stage

259
Q

How can you differentiate NASH vs NAFLD?

A

BIOPSY

260
Q

What is NAFLD? NASH?

A

NAFLD: fatty deposition in liver
NASH: fatty deposition in liver with INFLAMMATION

261
Q

Greater duration of NAFLD, age >50, postmenopausal WOMEN, HISPANICS/ASIANS, METABOLIC SYNDROME, persistent ALT elevation?

A

Greater risk for progression to NASH (metabolic syndrome is TOP risk predictor)

262
Q

What CLINICAL parameters can be looked at to predict NASH from NAFLD?

A

FIBROSIS studies (imaging - elastography), APRI, FIB-4 and ELF panel)

263
Q

Which CLINICAL test detects liver FIBROSIS by assessing AGE, Plt, AST/ALT?

A

FIB-4 (< 1.45 unlikely; >3.25 advanced)

264
Q

Non-FASTING, liver CONGESTION, AST/ALT fllare with HEPATITIS, and EXTRAHEPATIC BILIARY OBSTRUCTION are can all OVERESTIMATE results with this FIBROSIS test?

A

ELASTOGRAPHY (Fibroscan)

265
Q

What is the RATE of FIBROSIS progression in NAFLD/NASH?

A

NAFLD: 1 stage in 14 years
NASH: 1 stage in 7 years

266
Q

What should be done in a patient with NASH who has elevated LDL, triglycerides and ALT/AST?

A

Start STATINS (avoid CAD and cardiac death) - decreases ALT/AST in these patients

267
Q

Obese pt with METABOLIC syndrome, elevated LFTs, FERRITIN, LIPIDS, mild ANA, should be treated HOW if wt loss isn’t working?

A

Vitamin E (< 800 IU/day) - watch for prostate cancer and hemorrhagic stroke

268
Q

What FOOD item is BENEFICIAL in NAFLD?

A

COFFEE

269
Q

What is the MOST EFFECTIVE for FIBROSIS REGRESSION in NASH?

A

WEIGHT LOSS (at least 10% of body weight)

270
Q

At what BMI is BARIATRIC surgery recommended?

A

BMI >40
BMI >35 with obesity-related COMORBIDITIES

271
Q

Besides Vitamin E, what other medications are RECOMMENDED in patients with NASH and DM?

A

PIOGLITAZONE (edema, weight gain, bladder cancer and heart failure)
GLP-1 agonists (“utide/atide”)

272
Q

A DECREASE in ALT of what, is associated with HISTOLOGIC improvement of NALFD/NASH disease activity?

A

>17 U/L

273
Q

How does the HFE GENE (anomaly in HEMOCHROMATOSIS) regulate IRON?

A

By regulating HEPCIDIN which is what the liver uses to increase or decrease IRON ABSORPTION from the gut (enterocytes) via the ferroportin transporter

274
Q

Which TWO HFE genes are associated with hereditary HEMOCHROMATOSIS?

A

C282Y
H63D

275
Q

HIGH TRANSFERRIN saturation and HIGH serum FERRITIN, LOW HEPCIDIN age 40-50?

A

Hereditary HEMOCHROMATOSIS (C282Y/H63D) - Autosomal Recessive

276
Q

ANEMIA, parenchymal and SPLENIC IRON, HIGH HEPCIDIN (reduced iron export by MACROPHAGES)

A

FERROPORTIN disease (FPN gene - a type of hemochromatosis)

277
Q

Anemias such as Thalassemia, Sideroblastic, Sickle cell, Hemolysis, Spherocytosis, CHRONIC INFLAMMATION, EXCESS VIT C can lead to what condition?

A

Secondary IRON OVERLOAD

278
Q

Which genotype mutation is at HIGHEST RISK for developing an IRON OVERLOAD syndrome?

A

C282Y HOMOZYGOTE (TWO identical copies of a gene as in C282Y/C282Y)

279
Q
A
279
Q

Which POPULATIONS is HEREDITARY HEMOCHROMATOSIS highest in?

A

IRISH and SCANDINAVIANS

280
Q

Compound HETEROZYGOTE Hereditary Hemochromatosis such as C282Y/H63D can become IRON OVERLOADED when?

A

If COFACTOR present (alcohol, HCV, etc.)

281
Q

Do HETEROZYGOTE mutations of hereditary hemochromatosis or the H63D/H63D HOMOZYGOTE develop IRON OVERLOAD?

A

NO (only if cofactors present - alcohol, HVC, etc)

282
Q

Why does IRON OVERLOAD show up LATER in life in women?

A

Iron loss through MENSTRUATION

283
Q

Liver DISEASE, FATIGUE, in BRONZING, DM, GONADAL dysfunction, ARTHROPATHY (chondrocalcinosis), ARRHYTHMIAS, dilated CARDIOMYOPATHY are seen in this liver disroder?

A

Hereditary Hemochromatosis with IRON OVERLOAD

284
Q

How do you INITIALLY screen a SYMPTOMATIC, ASYMPTOMATIC (mildly elevated LFTs) or adult with 1st degree relative for HEREDITARY HEMOCHROMATOSIS?

A

Serum TRANSFERRIN (>45%), FERRITIN (>1000) and IRON SATURATION

285
Q

If a patient suspected of hereditary hemochromatosis has a TRANSFERRIN SATURATION >45%, what is the NEXT step?

A

Assess HFE GENOTYPE

286
Q

If HFE C282Y/C282Y HOMOZYGOTE, what do you ASSESS next?

A

FERRITIN and LFTs
If FERRITIN >1,000 and abnormal LFTs - BIOPSY staging
If FERRITIN < 1,000 and normal LFTs - PHLEBOTOMY

287
Q

If TRANSFERRIN saturation >45% BUT HFE genotype HETEROZYGOUS or COMPOUND HERETOZYGOUS (C282Y/H63D), what do you do next?

A

Assess serum FERRITIN
If FERRITIN >1,000 - PHLEBOTOMY
If FERRITIN normal - evaluagte for OTHER LIVER DISEASES/HEMATOLOGICAL disorders - BIOPSY

288
Q

```

~~~

If a patient with HFE mutation C282Y/C282Y HOMOZYGOUS presents with signs of CIRRHOSIS, what do you do?

A

Liver BIOPSY

289
Q

At what serum FERRITIN level do you sart TREATING (PHLEBOTOMY every 1-2 WEEKS) patients with HEREDITARY HEMOCHROMATOSIS with the C282Y/C282Y HOMOZYGOTE?

A

Women >200 ng/mL
Men >300 ng/mL

290
Q

What do you do for patients with HEREDITARY HEMOCHROMATOSIS with the C282Y/C282Y HOMOZYGOTE but with FERRITIN levels BELOW treatment (W < 200, M < 300)?

A

MONITOR LFTs and FERRITIN levels YEARLY

291
Q

What is the GOAL FERRITIN level for patients with HEREDITARY HEMOCHROMATOSIS with the C282Y/C282Y HOMOZYGOTE?

A

50 -100 ng/mL (once acieved, only need phlebotomy 3-4 x/yr)

292
Q

What VITAMIN should patients with HEREDITARY HEMOCHROMATOSIS with the C282Y/C282Y HOMOZYGOTE avoid?

A

Vit C (this vitamin helps ABSORB iron)

293
Q

Which FOOD can cause serious liver disease in a patient with HEREDITARY HEMOCHROMATOSIS with the C282Y/C282Y HOMOZYGOTE and should be AVOIDED?

A

SHELLFISH (VIBRIO)

294
Q

If PHLEBOTOMY is not possible for patients with HEREDITARY HEMOCHROMATOSIS with the C282Y/C282Y HOMOZYGOTE due to LIVER and RENAL TOXICITY, what can ONLY THEN be used instead?

A

Chelation agents (deferoxamine)

295
Q

What is CORRECTED with PHLEBOTOMY in patiens with HEREDITARY HEMOCHROMATOSIS with the C282Y/C282Y HOMOZYGOTE?

A

EARLY HEPATIC FIBROSIS, cardiac dysfunction, skin pigmentation, hepatomegaly, porphyria cutanea tarda (not the arthropathy, not DM, not hypogonadism)

296
Q

What is the amino acid substitution in patients with Alpha-1 Antitrypsin Deficiency (emphysema - COPD, liver disease in infants and children)

A

Glutamic Acid - to - Lysine in serine protease inhibitor A1 (SERPINA1) Z-ALLELE - autosomal dominant (M-allele is the normal one)

297
Q

What leads to the LIVER INJURY seen in patiens with Alpha-1 Antitrypsin Defficiency?

A

Abnormal POLYMERIZATION of Alpha-1 Antitrypsin molecules (can’t be excreted by the liver causing cell death)

298
Q

What is made if a patient has the NULL/NULL phenotype for Alpha-1 Antitrypsin?

A

NOTHING, no product also no liver disease (its only the poorly polymerized type that makes product tht cant be excreted out of the liver that caauses cell death) - only lung injury

299
Q

How do you CHECK for Alpha-1 Antitrypsin Defficiency?

A

PHENOTYPE (not the AT level as this changes with inflammation, underlying liver disease, etc.) MM normal, SS moderate ZZ severe and most COMMON

300
Q

Liver BIOPSY: PAS positive DIASTASE resistent globules?

A

Alpha-1 Antitrypsin Deficiency

301
Q

What is PRUSSIAN STAIN used for?

A

IRON OVERLOAD such as liver biopsy in patient with hereditary hemochromatosis

302
Q

Liver disease beginnign in INFANCY and CHILDHOOD with MILD AST/ALT elevation, ASCITES, CONJUGATED JAUNDICE, HEPATOMEGALY, VARICES?

A

Alpha-1 Antitrypsin Deficiency

303
Q

ALL patient who present with liver disease (abn LFTs, cirrhosis, PHTN, HCC) should be suspected to have A1AT and if ZZ allele positive, HOW OFTEN do you monitor (serology, imaging, elastography?

A

YEARLY

304
Q

What is the EXPRESSED state of A1AT (levels < 10)? CARRIER state (levles 50-100) - no disease unless concomitant liver disease? Normal levels 80-220

A

Expressed state: ZZ
Carrier state: MZ

305
Q

What is RECOMMENDED to patients with A1AT CARRIER state (MZ)?

A

Alcohol avoidance, reduction of metabolic risk factors, vaccines for HAV/HBV, smoking cessation

306
Q

This CLASS of drug should be AVOIDED in patients with A1AT Deficiency because it INCREASES production of the POORLY POLYMER MOLECULES?

A

NSAIDs

307
Q

What SCREENING is necessary for patients with A1AT Defficiency (ZZ allele)?

A

Screen for CIRRHOSIS, HCC, VARICES, PFT (lungs) and if decompensated, refer for TRANSPLANT

308
Q

YOUNG (< 45 yo), ACUTE liver failure, HIGH T.bili with LOW ALK PHOS, ANEMIA, ACUTE KIDNEY INJURY?

A

WILSON DISEASE

309
Q

Liver disease preceeds neurologic disease by 10 years, affects BRAIN, KIDNEY, HEART, CORNEA, ERYHTROCYTES, JOINTS?

A

WILSON DISEASE (hepatolenticular degeneration)

310
Q

Autosomal RECESSIVE, affects CHROMOSOME 13 ATP7B mutation and necesary for CERULOPLASMIN synthesis (LOW < 20 mg/dL)?

A

WILSON DISEASE (hepatolenticular degeneration)

311
Q

LIVER disease (LFTs, hepatitis, hepatomegaly, cirrhosis, ALF) + NEUROLOGIC disease (mania, psychosis, DEPRESSION, rigidity, seizures), COOMB’s negative HEMOLYTIC ANEMIA, INFERTILITY, OSTEOPOROSIS is suspicious for what?

A

WILSON DISEASE (hepatolenticular degeneration)

312
Q

Kaiser-Fleisher Rings & SUNFLOWER CATARACTS in the cornea suggest?

A

WILSON DISEASE (hepatolenticular deneneration) - slit lamp to visualize

313
Q

What CONFUSING findings are often seen on liver BIOPSIES of patients with WILSON DISEASE?

A

Features of FATTY liver and AIH

314
Q

What RENAL conditions does WILSON DISEASE cause besides AKI?

A

FANCONI syndrome (excessive drinking and urination), distal RTA and NEPHROTIC syndrome

315
Q

Coomb’s NEGATIVE hemolytic anemia, LOW alk phos, HIGH T.bili, AST»ALT, RENAL failure, < 45 yo, NEUROLOGIC disorders, LIVER TRANSPLANT is life saving?

A

WILSON DISEASE (hepatolenticular degeneration)

316
Q

Are NEUROLOGIC disorders REVERSIBLE in a patient with WILSON disease (liver transplant or otherwise)?

A

NO

317
Q

Serum CERULOPLASMIN < 20 mg/dL and 24-hour URINE COPPER >40 mcg are suggestive of?

A

WILSON DISEASE (if unsure, do LIVER BIOPSY)

318
Q

What COPPER-RICH foods should patients with WILSON disease avoid?

A

SHELLFISH, NUTS, CHOCOLATE, MUSHROOMS, ORGAN MEATS, PEAS, DRIED FRUIT

319
Q

How do you TREAT WILSON disease with meds?

A

Chelation (D-PENICILLAMINE + pyridoxine, TRIENTINE)
Decrease intestinal absorption: ZINC (nausea/vomiting/diarrhea)
SCREEN FAMILY

320
Q

When treating WILSON disease with chelator D-PENICILLAMINE, what can you see?

A

WORSENING of NEUROLOGIC symptoms (switch to TRIENTINE - also chelates iron so CAREFUL)

321
Q

When treating WILSON disease with chelator TRIENTINE, what can you NOT take with it as it forms a TOXIC complex?

A

IRON supplementation (trientine also chelates iron)

322
Q

CHILDHOOD, Autosomal DOMINANT, severe PRURITUS, HIGH GGT, JAG1 gene, abnormal FACE, BUTTERFLY vertebrae and PULMONIC stenosis?

A

ALLAGILE syndrome

323
Q

Focal or multilobular CIRRHOSIS, LUNG disease, can use URSO for cholestasis and optimize NUTRITION?

A

Cystic Fibrosis(CF)

324
Q

Genetic liver disease with either LOW GGT (types 1 & 2) - normal is 5-40 U/L or very HIGH GGT (type 3), HCC (type 2) INTRAHEPATIC GALLSTONES and massive BILE DUCT PROLIFERATION?

A

Progressive Familial Intrahepatic Cholestasis (PFIC)
If RELENTING and RELAPSING then (Benign Recurrent Intrahepatic Cholestasis) - BRIC

325
Q

Congestion/Cirrhosis in the liver causes back-up of blood in which VEIN reulting in ESOPHAGEAL/GASTRIC varices and splenomegaly?

A

PORTAL VEIN

326
Q

How is PRESSURE in the HEPATIC VEIN measured?

A

Wedge pressure

327
Q

CIRRHOSIS causes what KIND of PORTAL HTN?

A

SINUSOIDAL (therefore INCREASED Hepatic Vein Wedged Pressure) - normal Free HV pressure and INCREASED gradient
HVPG = WHPV - FHVP

328
Q

Does PORTAL VEIN THROMBOSIS affect the Hepatic Vein Pressure Gradient?

A

NO (the hepatic vein is wedged not the portal)

329
Q

What is considered CLINICALLY-SIGNIFICANT portal HTN (development of ascites or beeding varices)?

A

Hepatic Vein Pressure Gradient (HVPG >10 mmHg)

330
Q

How do you NON-IVASIVELY determine presence or portal HTN?

A

Vibration ELASTOGRAPHY with >20 kPa & Plt < 150K

331
Q

Portosystemic COLLATERALS found on imaging or UMBILICAL VEIN (round ligament of liver) mean what?

A

Portal HTN

332
Q

How do you PROPHYLACTICALLY treat a patient with CLINICALLY-SIGNIFICANT portal HTN (HVPG >20 mmHg)?

A

NON-SELECTIVE beta-blockers (propranolol, nadolol, carvedilol) - prevents ascites, variceal BLEEDING, encephalopathy

332
Q
A
333
Q

What is the most COMMON complication of cirrhosis?

A

ASCITES (5-year 44% mortality)

334
Q

What MAP is assocciated with increased SURVIVAL for patients with ASCITES?

A

MAP >82 mmHg

335
Q
A
335
Q

Calculate SAAG?

A

SAAG = Serum Alb - Asctites Alb
If >1.1 g/dL can be cirrhosis or RIGHT HEART / Budd Chiari (if < 1.1 - likely peritoneal cancer, TB, etc.)

If Ascites Protein < 2.5 g/dL = CIRRHOSIS if >2.5 g/dL do HV doppler or ECHO

336
Q

Do you REPEAT a SAAG after it has been obtained?

A

NO (same result)

337
Q

What do you ALWAYS order on a patient with FIRST ONSET ASCITES?

A

SAAG, PMN, CULTURE, PROTEIN

338
Q

What do you ALWAYS order for a patient with ASCITES wheter first episode or recurret or whetehr inpatient or outpatient?

A

PMN (rule out SBP >250)

339
Q

What do you order for an INPATIENT ONLY, with ASCITES whetehr first episode or recurrent?

A

CULTURE

340
Q

When do you order CYTOLOGY in a patient with ASCITES?

A

If SAAG < 1.1 and suspect cancer

341
Q

When do you order TRIGLYCERIDES in a patient with ASCITES?

A

If ASCITES is MILKY WHITE (chylous, >110 mg/dL)

342
Q

If ASCITES is found on CULTURE to be POLYMICROBIAL, CEA >5 ng/mL, ALK PHOS >240 U/L, what does this indicate?

A

Gut PERFORATION

343
Q

If AMYLASE >100 is found in ASCITES, what is it from?

A

PANCREATIC ascites (needs imaging/ERCP)

344
Q

SAAG >1.1 Ascites TP >2.5 what ELSE can you check before commiting to CARDIAC source instead of Budd-Chiari?

A

pro-BNP >6,100 pg/m
(its only 166 pg/mL in cirrhosis)

345
Q

Is CA-125 test helpful for ASCITES?

A

NO

346
Q

ASCITES that is RESPONSIVE to LOW-SODIUM diet and DIURETICS?

A

GRADE-1 (does not require paracentesis)

346
Q

RECURRENT ASCITES (3 or more times/year) in spite of SODIUM RESTRICTION ans DUIRETICS with MODERATE abdomina distension?

A

GRADE-2 (consider LVP/TIPS)

347
Q

RECURRENT LARGE-VOLUME ASCITES with SEVERE abdominal distention, refractory to sodium restriction and diuretics and recurrs EARLY post PARACENTESIS (requires frequent paracentesis)?

A

GRADE-3 (refractory) - TIPS

348
Q

INITIAL considerations and treatment of ASCITES?

A

Sodium-restric diet (< 2 g/day)
AVOID ACE-I & ARBs (increase renal failure and HYPOtension
Spironolactone 100 mg/day + Furosemide 40 mg/day (increase as needed 2.5:1 ratio)

349
Q

In a patient with ASCITES who is treated with SPIRONOLACTONE and develops GYNECOMASTIA, what do you replace with?

A

Eplerenone or Amiloride

350
Q

At what Cr level do you REDUCE or STOP DIURETICS for ASCITES?

A

>1.5 mg/dL

351
Q

A SPOT Urine Na:Urine K >1 means what in patients with ASCITES?

A

DIETARY non-compliance

352
Q

When should ALBUMIN be given to patients whom undergo LVP for ASCITES?

A

When removing >5 L

353
Q

In patients requiring recurrent LVP (weekly) with evidence of KIDNEY INJURY (Cr >1.5), what should be considered?

A

TIPS

354
Q

What is the preferred medication for treatment of MUSCLE CRAMPS in patients with ASCITES?

A

BACLOFEN

355
Q

REFRACTORY ASCITES, HEPATIC HYDROTHORAX (ascites that migrates to become pleural fluid) and ACUTE UNCONTROLLED or RECURRENT VARICEAL BLEEDING are all indications for what?

A

TIPS

356
Q

Pulmonary HTN, PRIMARY prevention of variceal bleeding, SEVERE CHF (stage C, D), SEPSIS, active BILIARY OBSTRUCTION, TUMOR preventing placement, REFRACTORY HE are all ABSOLUTE CONTRAINDICATIONS to what?

A

TIPS

357
Q

What are the three (3) RELATIVE contraindications to TIPS?

A

Decompensated CIRRHOSIS (liver won’t handle the shunt well):
1. MELD >18
2. T.bili >4
3. INR >5

358
Q

Pt s/p TIPS, presents with PERSISTENT ASCITES >6 weeks after TIPS placement, whats the issue?

A

TIPS dysfunction

359
Q

If a patient has had >3 LVP in ONE YEAR, what is recommended?

A

TIPS

360
Q

Pt comes in with ASCITES, PMN < 250 but blood cultures positive, NO SIGNS of infection otherwise, how do you TREAT?

A

NO ANTIBIOTICS, repeat diagnostic paracentesis (contamination)

361
Q

Is PRIMARY PROPHYLAXIS (BEFORE it occurs) for SBP standard of care for pts with ASCITES?

A

NO (risk of developing resistent infection)

362
Q

What is the TREATMENT of SVP?

A

IV ANTIBIOTICS (cephalosporins, quinolones) + IV ALBUMIN (3 days) - 19% MORTALITY REDUCTION with combination therapy

363
Q

In a patient with ASCITES and SBP, what treatments should be AVOIDED?

A

Aggressive DIURESIS, LVP, IV CONTRAST, HOLD beta-blockers (hypotension, AKI)

364
Q

How LONG is SBP treated for?

A

7 DAYS (repeat paracentesis on day 3 if fever/pain persist)

365
Q

In a patient being TREATED for SBP, PMNs are found to be >PRETREATMENT value, what should be SUSPECTED?

A

RESISTENT organism or SURGICAL source

366
Q

In a patient being treated for SBP, the PMNs are found to still be ELEVATED, but < PRETREATMENT value, what do you do?

A

CONTINUE treatment for an additional 48 HOURS, then REPEAT PARACENTESIS

367
Q

WHEN is PROPHYLAXIS for SBP considered STANDARD of care?

A

ONLY after FIRST EPISODE of SBP (otherwise recurrence is 70%)

368
Q

What is appropriate prophylaxis for SBP?

A

DAILY (not weekly) CIPRO, or NORFLOXACIN, or BACTRIM

369
Q

**

If a patient presents with ASCITES, CIRRHOSIS and GIB, what do you give for SBP PROPHYLAXIS?

A

CEFTRIAXONE 1 g IV DAILY x 7 days

370
Q

Is treating CIRRHOSIS with ALBUMIN in inpatients helpful?

A

NO (not unless they have SBP or undergo LVP)

371
Q

In CIRRHOTICS with ASCITES, OVERDIURESIS, dehydration due to LACTULOSE (HE), LVP, SBP, GIB, beta-blockers, NSAIDs, INFECTION all can LEAD TO?

A

HEPATORENAL SYNDROME (HRS-AKI/CKI)

372
Q

What are the HRS-AKI STAGES?

A

Stage 1: Increase of Cr by 0.3 mg/dL/BASELINE - 2xBASELINE
Stage 2: Increase of Cr by 2-3xBASELINE
Stage 3: Increase of Cr by >3xBASELINE or >4.0 mg/dL

373
Q

What are the three (3) kinds of AKI in a patient with CIRRHOSIS with ASCITES?

A

TRANSIENT (returns to baseline)
PERSISTENT (Cr increase >0.3 mg/dL over 48H, no dialysis)
PROGRESSIVE (persistent AKI requiring dialysis)

374
Q

How is HRS treated?

A

STOP anti-hypertensives, use OCTREOTIDE + MIDODRINE + ALBUMIN, NOREPINEPHRINE, TERLIPRESSIN (can cause resp failure)

375
Q

Is DOPAMINE used to treat HRS?

A

NO

376
Q

When using TERLIPRESSIN to treat HRS, what MUST you watch for?

A

REPIRATORY FAILURE (do not start on patients who have respiratory compromise)

377
Q

What kind of HYPONATREMIA can a patient on DIURETICS and LACTULOSE have and how is it TREATED?

A

HYPOVOLEMIC (NS + IV Albumin) do NOT volume restrict

378
Q

What are the three (3) stages of HYPOnatremia and how do you TREAT?

A

MILD: 126-135 mEq/L - monitor, water restrict if HYPERvolemic
MODERATE: 120- 125 mEq/L - water restrict to 1L/day, STOP diuretics
SEVERE: < 120 mEq/L - water restrict to 1L/day, stop diuretics, IV albumin

379
Q

WHEN is HYPERTONIC (3% NS) SALINE (or RARELY satavaptan or tolvaptan) used to treat HYPOnatremia?

A

Short-term for SYMPTOMATIC or imminant liver TRANSPLANT (goal is 4-6 mEq/L in 24 hours, NO MORE than 8 mEq/L in 24 hours)

380
Q

A CIRRHOTIC patient presents with SUSPICION of esophageal VARICES but liver STIFFNESS is < 20 kPa and Plt >150K, how do you proceed?

A

NO EGD NECESSARY

381
Q

What is the 5-YEAR mortality risk of a patient with CIRRHOSIS with VARICEAL BLEED?

A

20%

382
Q

What does VARICEAL BLEED (not the presence of varices) mean for pt’s CIRRHOSIS?

A

DECOMPENSATED cirrhosis

383
Q

What is considered NORMAL HVPG?

A

3-5 mmHg

384
Q

What is considered CLINICALLY SIGNIFICANT HVPG?

A

>10 mmHg

385
Q

At what HVPG is there a risk of VARICEAL BLEEDING?

A

>12 mmHg

386
Q

At what HVPG is there a risk of DEATH?

A

>16 mmHg

387
Q

At what HVPG is there a risk of being UNABLE to STOP VARICEAL BLEEDING?

A

>20 mmHg

388
Q

Do NON-SELECTIVE beta-blockers PREVENT formation of esophageal VARICES?

A

NO

389
Q

Once esophageal VARICES are there, what is used for PRIMARY PROPHYLAXIS?

A

NON-SELECTIVE beta-blockers (nadolol, propranolol, carvedilol)

390
Q

Once esophageal VARICES BLEED, what is used for SECONDARY PROPHYLAXIS?

A

Band LIGATION (60% recureence if not)

391
Q

How OFTEN do you SCREEN for esopahgeal VARICES in a cirrhotic patient, that have NEVER BLED if NO VARICES on FIRST EGD?

A

Every 2 YEARS if ACTIVE disease (drinks, active viral hep)
Every 3 YEARS if INACTIVE
IMMEDIATELY if presents with DECOMPENSATED CIRRHOSIS

392
Q

WHEN do you perform an EGD on ANY patient who presents with DECOMPENSATED CIRRHOSIS (variceal bleed, jaundice, ascites, HE)?

A

IMMEDIATELY

393
Q

If a patient with CIRRHOSIS presents with variceal bleed, or jaundice, or ascites or HE, what TYPE of CIRRHOSIS do they have?

A

DECOMPENSATED cirrhosis

394
Q

How OFTEN do you SCREEN for esopahgeal VARICES in a cirrhotic patient, that have NEVER BLED if SMALL VARICES on FIRST EGD?

A

Every 1 YEAR if ACTIVE disease (drinks, active viral hep)
Every 2 YEARS if INACTIVE
IMMEDIATELY if presents with DECOMPENSATED CIRRHOSIS

395
Q

How OFTEN do you SCREEN for esopahgeal VARICES in a cirrhotic patient, that have NEVER BLED if MEDIUM/LARGE VARICES on FIRST EGD?

A

NON-SELECTIVE beta-blockers or EGD with BANDING (every 2 weeks until eradicated) but NOT BOTH

396
Q

When do you start PRIMARY PROPHYLAXIS for esophageal VARICES with non-selective beta-blockers OR banding but NOT BOTH?

A

MEDIUM-LARGE varices or SMALL (with red-whale sign)

397
Q

Should Nitrates or Sclerotherapy be used for primary prophylaxis of esophageal varices?

A

NO

398
Q

WHEN is it RECOMMENDED to use BOTH non-selective beta-blockers and EGD with BANDING for esophageal variceal bleed prophylaxis?

A

For SECONDARY PROPHYLAXIS (already bled once)

399
Q

What are the REQUIRED elements for management of ACUTE variceal BLEEDING?

A
  1. Early EGD in 12 HOURS
  2. OCTREOTIDE x 72 HOURS
  3. PPI x 10-14 DAYS ONLY (stabilizes clot)
  4. Prophylactic Abx (CEFTRIAXONE) x 7 DAYS
400
Q

Do long-term PPIs PREVENT variceal BLEEDING?

A

NO

401
Q

How FREQUENTLY do you REPEAT EGDs after initial variceal BLEED?

A

Every 2 WEEKS until eradicated
Then screen again in 3 MONTHS
If NONE, then in 6-12 MONTHS

402
Q

WHEN should TIPS be recommended in variceal BLEEDING?

A

EARLY - within 72 HOURS (better survival and less bleeding episodes)
10 mm TIPS is better than larger, less complications

403
Q

Which GASTRIC varices CAN be BANDED?

A

GastroEsophaealVarices 1&2 (GOV 1&2)

404
Q

Which GASTRIC varices CANNOT be BANDED (Minnesota tube, Octreotide, TIPS)?

A

IsolatedGastricVarices 1&2 (IGV 1&2)

405
Q

What type of IMMAGING is recommended post esophageal variceal HEMOSTASIS?

A

CROSS-SECTIONAL (determine vascular anatomy)

406
Q

What type of ENDOSCOPIC therapy is RECOMMENDED for GASTRIC VARICES (IGV 1&2)?

A

EUS-GUIDED CYANOACRYLATE NON-LIPOIDAL

407
Q

In GASTRIC VARICES, if these are MAINLY FED by the CORONARY VEIN, what is the preferred mode of TREATMENT?

A

TIPS

408
Q

In GASTRIC VARICES, if these are MAINLY FED by a GASTRO-RENAL SHUNT, what is the preferred mode of TREATMENT?

A

BRTO (Balloon-occluded Retrograde Transvenous Obliteration) - as long as no ASCITES or HE

409
Q

What medications can PRECIPITATE HE?

A

Benzodiazepines, Narcotics, Gabapentin, Mirtazapine

410
Q

Besides cleaning-up a pt’s medication list, how do you TREAT HE?

A

Lactulose (titrate 1-3 soft BMs/day)
Add RIFAXIMINE if insufficient
Correct HYPOnatremia
HIGH-PROTEIN diet (1.2-1.5 g/kg/day with late-night snack)

411
Q

What can be PRECIPITATED after TIPS and how do you TREAT prophylactically?

A

HE - RIFAXIMIN

412
Q

An OUTPATIENT with established cirrhosis and ascites presents for LVP, what shuld be sent?

A

PMNs ONLY (if inpatient, PMNs and culture)

413
Q

If a CIRRHOTIC patient presents with PVT, what do you check for?

A

CANCER (liver, cholangio, pancreas) - CONTRAST CT

414
Q

If a patient WITHOUT cirrhosis patient presents with PVT, what do you check for?

A

SURGERY, MYELOPROLIFERATIVE disorder, THROMBOPHILIA (V617, JAK2)

415
Q

Is PVT caused by MALIGNANCY treated with ANTICOAGULATION?

A

NO

416
Q

Clots caused by a MALIGNANCY are different on IMAGING than NON-MALIGNANT clots how?

A

These ENHANCE and look whiter than “bland clots” that look gray

417
Q

How LONG do you ANTICOAGULATE a non-malignant ACUTE PVT?

A

3-6 MONTHS

418
Q

How LONG do you ANTICOAGULATE a CHRONIC PVT?

A

You DON’T unless (extends to SMV, causes bowe ISCHEMIA or caused by a thrombophilia - JAK2 or V617)

419
Q

COLLATERAL formation around a PVT indicates what?

A

CHRONIC PVT (do NOT anticoagulate)

420
Q

What MUST be done for ALL CHRONIC PVT pts?

A

EGD to rule out varices

421
Q

WHEN are the ONLY 2 OCCASIONS where PVT is NOT anticoagulated?

A

MALIGNANCY and if causes PARTIAL obstruction

422
Q

What part of the liver ENARGES with BUDD-CHIARI syndrome and why?

A

CAUDATE LOBE (segment 1) - due to collaterals formed - which can result in compression of the IVC

423
Q

In which CONDITION do you see ENHANCING nodules in the liver that are NOT HCC but rather REGENERATIVE (should be BIOPSIED)?

A

BUDD-CHIARY syndrome

424
Q

What is the WORKUP and TREATMENT of BUDD-CHIARI syndrome?

A

Evaluate for THROMBOPHILIA (JAK2 or V617) and start HEPARIN, LMWH, Direct Oral Anticoagulants, WARFARIN

425
Q
A
426
Q

When is TIPS or liver TRANSPLANT considered for a patient with BUDD-CHIARI syndrome?

A

LIVER FAILURE

427
Q

This condition APPEARS as BUDD-CHIARI syndrome but is caused by occlussion of SMALL intrahepatic vessels not large ones (hepatic veins PATENT on imaging), presents with PAIN, WEIGHT GAIN and ASCITES, caused by CHEMOTHERAPY, AZATHIOPRINE. How is it TREATED?

A

Sinusoidal Occlusive Syndrome (SOS)
Prevent with URSO
Treat with DEFIBROTIDE

428
Q

Should you CORRECT thrombocytopenia or a coagulopathy (elevated INR) for LOW-RISK procedures (paracentesis, thoracentesis, EGD w/banding)?

A

NO

429
Q

What can be used for HEMOSTASIS in patiets with CIRRHOSIS and LIVER FAILURE?

A

DESMOPRESSIN (DDAVP)

430
Q
A
430
Q

What is given to patients with symptomatic DVT or portal or mesenteric vein THROMBOSIS?

A

IV HEPARIN

431
Q

What should raise SUSPICION of CARDIAC etiology of ASCITES?

A

SAAG >1.1 g/dL & ASCITES PROTEIN >2.5 g/dL

432
Q

Whar are the CARDIAC etiologies of ASCITES (protein >2.5)?

A

Constrictive pericarditis (need cardiac MRI to diagnose)
RIGHT heart failure
Pulmonary HTN
TRICUSPID insufficiency

433
Q

How do you TREAT ascites caused by CARDIAC etiology?

A

Treat underlying heart disease (diuretics can result in hypotension and shock)

434
Q

In ISCHEMIC hepatitis, why does the BILIRUBIN still rise for a week or more after AST/ALT decline?

A

LAG (but it will normalize ~2 weeks)

435
Q

RECURRENT, spontaneous nose bleeds, skin telangiectasias, involves GIT, LUNGS & BRAIN, Family History, HH1 MUTATION (endoglin ENG)?

A

Hereditary Hemorrhagic Telangiectasia (HHT) or Osler-Weber-Rendu syndrome

436
Q

What do you do for a patient with HHT as far as screening and treatment?

A

Treat by REPLETING IRON, embolize SYMPTOMATIC PULMONARY AVMs, and cerebral AVM screening with CT/MRI?

437
Q

How do you treat SYMPTOMATIC HEPATIC AVMs?

A

BEVACIZUMAB

438
Q

VASCULAR injury to liver or casued by AZATHIOPRINE, STENOSIS of intrehepatic VEINS, appears like CIRRHOSIS on imaging but is not. HPVG is normal but with portal HTN?

A

Nodular Regenerative Hyperplasia (NRH)

439
Q

Randomly distributed BLOOD FILLED CAVITIES in the liver caused by AZATHIOPRINE, HIV, BARTONELLA, ANABOLIC STEROIDS, multiple myeloma or Hodgkin’s?

A

PELIOSIS Hepatitis

440
Q

If a THROMBUS ENHANCES on arterial phase, it is most likely caused by what? How do you NOT treat?

A

MALIGNANCY - do NOT anticoagulate

441
Q

ASCITIC fluid PROTEIN >2.5 mg/dL?

A

CARDIAC or Budd-Chiari (NO DIURETICS)

442
Q

Do hepatic SIMPLE CYSTS cause SYMPTOMS?

A

Only if LARGE and COMPRESS stomach or organs

443
Q

If you find >10-20 hepatic CYSTS in a patient, what should you SUSPECT?

A

POLYCYSTIC liver/kidney disease (AD PRKCSH or SEC63 genes)

444
Q

If a hepatic CYST sppears NODULAR or has internal SEPTATIONS?

A

RESECT (15% cancer risk - biliary cytadenomas)

445
Q

When is the ONLY time HEMANGIOMAS require surgical intervention?

A

When they cause SYMPTOMS or HIGH-OUTPUT HF, or THROMBOCYTOPENIA, DIC and SYSTEMIC BLEEDING?

446
Q

CENTRIPETAL ENHANCEMENT of a lesion on MRI?

A

HEMANGIOMA (bening regardless of size)

447
Q

FEMALE, SOLITARY LIVER LESION < 5 cm, CENTRAL SCAR?

A

FOCAL NODULAR HYPERPLASIA (not associated with OCPs or estrogen) - BENIGN

448
Q

ISOINTENSE lesion on T2 MRI phase with CENTRAL SCAR?

A

FOCAL NODULAR HYPERPLASIA (FNH)

449
Q

These liver TUMORS (HNF-apha) are usually found in the RIGHT lobe, are SOLITARY, lack bile ducts or normal architecture, are associated with OCPs and PCOS, risk of HEMORRHAGE and MALIGNANT (BETA-CATENIN) transformation? Treatment?

A

Hepatic ADENOMAS
Stop OCPs, observe, RESECT/ABLATE (if found in men, or if enlarging)

450
Q

ALL ASIAN men (>40), women (>50) and ANY individuals who are Hep B CARRIERS and have a FAMILY HISTORY of this, should undergo SURVEILLANCE?

A

HCC (US and AFP every 6 MONTHS)

451
Q

What should ALL BLACKS with HBV undergo surveillane for?

A

HCC (US and AFP every 6 MONTHS)

452
Q

ALL patients with CIRRHOSIS (HBV, HCV, PBC, hemochromatosis, alpha-1, etc) should undergo SURVEILLANCE for?

A

HCC (US and AFP every 6 MONTHS)

453
Q

How is HCC NON-INVASIVELY DIAGNOSED?

A

CT or MRI, lesion >2 cm with LATE ARTERIAL ENHANCEMENT & PORTAL VENOUS WHASHOUT (LIRADS-5) no biopsy needed

454
Q

Why are most patients with HCC NOT candidates for surgical RESECTION?

A

Because they are CIRRHOTIC and lack liver reserve

455
Q

In patients with HCC not candidates for LOCOREGIONAL therapy, or RESECTION or due to METASTATIC disease ot CIRRHOSIS, what is the treatment?

A

ATEZOlizumab + BEVAcizumab (others are sorafenib, levatinib)

456
Q

BEFORE treating for HCC or HHT with BEVAcizumab, what should be DONE first?

A

EGD to evaluate and treat VARICES (GIB risk)

457
Q

Is SORAFENIB therapy preferred for treatment of HCC or for adjuvant therapy after resection or LocoRegionalTherapy?

A

NO

458
Q

Decribe the MILAN criteria for TRANSPLANT eligibiltiy for a patient with HCC?

A

ONE lesion < 5 cm or Up to THREE lesions < 3 cm EACH

459
Q

What is the UCSF criteria for DOWNSTAGING to MILAN criteria for liver TRANSPANT for a patient with HCC?

A

ONE lesion >5 cm but < 8 cm
TWO-FIVE lesions each < 5 cm but COLLECTIVELY < 8 cm

460
Q

The ONSET of HE within 8 WEEKS of FIRST symptoms of LIVER DISEASE suggests what?

A

Acute Liver Failure (ALF) - no pre-existing liver disease

461
Q

What does the presence of HEPATIC ENCEPHALOPAHTY mean?

A

LIVER FAILURE

462
Q

What is REQUIRED CRITERIA for a STATUS 1A (highest status for requirement of immediate LIVER TRANSPLANT for ACUTE (not acut on chronic) Liver Filure?

A

ICU care required
VENTILATED
On DIALYSIS
INR >2

463
Q

In a patient with ACETAMINOHEN OD, what is the KING’s COLLEGE CRITERIA for the WORST PROGNOSIS (TRANSPLANT IMPENDING)?

A

Arterial pH < 7.30
INR >6.5 (PT >100)
Cr >3.4
HE Grade 3-4

464
Q

Patient presents with AST/ALT in the THOUSANDS and BILI is NORMAL, no alcohol nor acetaminophen history, no ischemia?

A

HERPES Hepatitis (test with PCR, treat with acyclovir)

465
Q

What is BENEFICIAL to start for ANY patient with ACUTE LIVER FAILURE (presence of HE) regardless of etiology?

A

N-cetylcysteine

466
Q

What are the INDICATIONS for liver TRANSPLANT?

A

MELD-Na >15
DECOMPENSATED CIRRHOSIS
MELD EXCEPTION (HCC - MILAN or USCF downgraded)

467
Q
A
468
Q

What are the MELD EXCEPTIONS for liver TRANSPLANT?

A

HCC (MILAN or USCF downgrade)
HepatoPulmonary Syndrome
Cholangiocarcinoma
Cystic Fibrosis
Refractory Cholangitis

469
Q

Which are the TWO PULMONARY conditions associated with portal HTN and CIRRHOSIS?

A

Portopulmonary HTN - ECHO, RIGHT heart CATH
Hepatopulmonary Syndrome - RIGHT to LEFT SHUNT (bubble ECHO)

470
Q

What is the MOST COMMON infection after LIVER TRANSPLANT?

A

CMV (highest risk is 3 MO post transplant)
FEVER, N/V/D - PCR

471
Q

MAJOR Adverse Effect of Cyclosporine & Tacrolimus?

A

Chronic KIDNEY Injury

472
Q

MAJOR Adverse Effect of EVEROLIMUS/SEROLIMUS?

A

ANEMIA, HYPERlipidemia

473
Q

MAJOR Adverse Effect of Mycophenolate Mofetil?

A

TERATOGEN
ANEMIA, DIARRHEA, CMV

474
Q

Which MEDS INCREASE levels of TACROLIMUS/CYCLOSPORINE?

A

Antifungals (ketoconazole, fluconazole)
Metoclorpamide
HIV drugs (protease inhibitors)

475
Q

Which MEDS DECREASE levels of TACROLIMUS/CYCLOSPORINE?

A

TB drugs, anti-SEIZURE

476
Q

What does AMIODARONE + SOFOSBUVIR (HAART) cause?

A

Cardiac Issues

477
Q

What are the COMMON cancers seen post LIVER TRANSPLANT?

A

SKIN (squamous/basal cell)
KAPOSI Sarcoma HHV-8
COLON (if for PSC)
OROPHARYNX (if for EtOH cirrhosis)

478
Q

Patient with EtOH cirrhosis comes in with a 50% occlusive PVT that arterially enhances on CT but no mass is shown, next step?

A

AFP (because if >200 ng/mL its HCC)

479
Q

How do you MONITOR a patient on METHOTREXATE (should ABSTAIN from alcohol) for development of liver disease?

A

Annual ELASTOGRAPHY (DILI and fibrosis)

480
Q

What is the PREFERRED analgesic in pts with CIRRHOSIS?

A

ACETAMINOPHEN

481
Q

When do you perform an EGD after a patient underwent BRTO for bleeding VRICES?

A

2-4 WEEKS

481
Q

In a patient with CIRRHOSIS and a VARICEAL BLEED, what is the PREFERRED treatment where there is ANY “TYPE b” (gastro-renal shunt) anatomy?

A

BRTO (Balloon Retrograde Trans-Obliteration)

482
Q

What does the presence of ASCTIES tell you about the pt’s CIRRHOSIS?

A

DECOMPENSATED cirrhosis (Child B or C)

483
Q

In an active Hep C (G 1-6) patient with DECOMPENSARED cirrhosis (ascites, etc), what is the treatment regimen?

A

12 WEEKS SOFOSbuvir + VELpatasvir + RIBAvirin (or 24 WEEKS without RIBA)

484
Q

Which Hep C drugs (protease inhibitors) CANNOT be used with DECOMPENSATED CIRRHOSIS (ascites, etc.)?

A

VOXilaprevir and GLEcaprevir

485
Q

What is IMPORTANT to test for in a patient with Hep C GENOTYPE 3, PRIOR to initiating treatment?

A

Y93H mutation (reduced SVR)

486
Q

In a patient with DECOMPENSATED CIRRHOSIS who presents with PANCYTOPENIA, ATAXIA and HYPERcholesterolemia, what is the DEFFICIENCY?

A

COPPER

487
Q

Night blindness is associated with which defficiency?

A

Vitamin A

488
Q

Cardiomyopathy, myositis, cramps and alopecia are associated with which defficiency?

A

SELENIUM

489
Q

If a patient receiving treatment for Hep C and is doing well, but LFTs become HIGHLY elevated, what shoud you SUSPECT?

A

Re-activation of Hep B (check HBsAg, HBc IgM, DNA)

490
Q

If a patient with Hep C presents and looks like he might clear the virus spontaneouslty, do you wait or do you treat?

A

TREAT ASAP (to clear viral load right away) do NOT WAIT

491
Q

If a pt with Hep C requires TRANSPLANT (liver, kidney, etc) what MUST you check first before treatment?

A

If he CONSENTED to Hep C POSITIVE donor (because he would get the transplant much quicker then treat)

492
Q

In a patient with CHRONIC Hep B treated with DAA with HBsAg+ and undetectable DNA and HBeAg- who asks if they can STOP therapy, WHAT predicts HBsAg LOSS after stopping therapy?

A

HBsAg QUANTITATIVE TITER (not HBeAb)
If < 100, good chance for spontaneous clearance

493
Q
A
494
Q

In a patient with a PVT with EXTENSION into SMV who had their last EGD >1 year ago with NO VARICES, who is listed for LIVER TRANSPLANT, what do you do BEFORE starting ANTICOAGULATION?

A

REPEAT EGD to evalaute for varices PRIROR to TRANSPLANT

495
Q

Acute CHOLESTASIS of PREGNANCY with PRURITUS, elevated ALK PHOS, elevated serum BILE ACIDS can safely be TREATED with what?

A

URSO

496
Q

If a patient is foud to have Focal Nodular Hyperplasia (central scar) on imaging, what is the follow-up?

A

NOTHING else needs to be done

497
Q
A
498
Q

This DRUG causes DILI which looks like AIH (AST/ALT&raquo_space; ALK PHOS), treatmet is STOPPING the drug.

A

MINOCYCLINE, STATINS, nitrofurantoin, methyldopa, hydralazine, DICLOFENAC, MELOXICAM, anendronate

499
Q

If a patient is HBsAG+ or HBcAb+ and undergo IMMUNOSUPPRESSIVE or CHEMOTHERAPY require WHAT?

A

ORAL antiviral therapy while treated and for 12 MONTHS after completion

500
Q

If a Hep B patient is about to be started on TENOFOVIR, what MUST they be tested for BEFORE starting therapy and why?

A

HIV (because tenofovir can cause treatment to be ineffective for HIV)

501
Q

If a patient responds well to prednisone and AZATHIOPRINE with LFT normalization then LFTs start going up again (ALT/AST), what do you need to check?

A

THIOPURINE metabolities from azathioprine toxicity - check 6-MMP

502
Q

Most COMMON reason for elevation of ALK PHOS and PRURITUS post liver TRANSPLANT (even YEARS later) and what do you do to diagnose?

A

Biliary ANASTOMOTIC STRICTURE - do ERCP

503
Q

What is the most CONSISTENT and REPRODUCIBLE method used to quantfy MUSCLE MASS (such as in a patient with sarcopenia and fraily awaiting liver transplant)?

A

CT for Skeletal Muscle Index

504
Q

In a CIRRHOTIC patient with Mental Status Changes and Confusion, if BLOOD VENOUS AMMONIA levels are NORMAL, whats the issue?

A

NOT HE, may be metabolic or different etiology

505
Q
A
505
Q

Patient with CIRRHOSIS and gastric bypass presents with RASH, ALOPECIA, HE and MYOPATHY, what is their DEFFICIENCY?

A

ZINC

506
Q
A
507
Q

SELENIUM DEFFICIENCY results in what condition?

A

CARDIOMYOPATHY

508
Q

COPPER DEFFICIENCY results in what conditions?

A

HYPERlipidemia, BONE MARROW SUPPRESSION

509
Q

Hepatopulmonary syndrome with a RA SpO2 of < 60 mmHg is considered HOW in terms of liver TRANSPLANT priority?

A

This is a MELD EXCEPTION and would be PRIORITIZED

510
Q
A
511
Q

Ptients with ACUTE Liver Failure should be ROUTINELY TESTED for what?

A

HERPES (HSV)

512
Q

What is the FIRST LINE TREATMENT of HCC that is unresectable?

A

ATEZolizumab + BEVacizumab

513
Q

Patient presenting with bloody DIARRHEA and FEVER after a liver TRANSPLANT on immunosuppressive therapy needs to be checked for?

A

CMV (PCR)

514
Q

Which is one of the ONLY scenarios in which N-acetylcysteine is NOT recommended?

A

CHILDREN with non-acetaminophen DILI (harmful)

515
Q

Which feature on HISTOLOGY is the most important in predicting LIVER-rlated outomes?

A

Stage of FIBROSIS

516
Q

In a CIRRHOTIC patient with HCC about to start CHEMOTHERAPY (ATEZolizumab + BEVacizumab), what MUST be done first?

A

EGD to rule out VARICES (because the adeverse effects of ATEZolizumab + BEVacizumab are GI bleed)

GI Boards November 20th 2024 (11 decks)

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